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Updated: Mar 29, 2026

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
Approaches to Improving Cardiac Structure and Function During and After an Acute Myocardial Infarction: Acute and
Robert A Kloner1, Wangde Dai2, Sharon L Hale3
1HMRI Cardiovascular Research Institute, Huntington Medical Research Institutes, Pasadena, California, USA Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA Guest Editor: Jonathan Leor kloner@hmri.org.
Insights
Myocardial infarction (MI) remains a significant health issue. New therapies are needed to reduce heart damage during ischemia and improve cardiac structure and function post-MI.
Area of Science:
- Cardiology
- Regenerative Medicine
Background:
- Myocardial infarction (MI) continues to cause significant mortality and morbidity despite advancements in reperfusion therapy.
- Current strategies targeting reperfusion injury have shown limited clinical success in acute ST-segment elevation myocardial infarction.
- Reducing myocardial cell death during ischemia is crucial for limiting infarct size.
Purpose of the Study:
- To explore therapeutic strategies for reducing myocardial infarct size.
- To investigate methods for mitigating adverse left ventricular remodeling post-MI.
- To identify optimal approaches for preserving cardiac structure and function after infarction.
Main Methods:
- Review of current therapeutic approaches for myocardial infarction.
- Discussion of strategies targeting ischemic cell death.
- Exploration of regenerative cardiology principles, including cellular and non-cellular therapies.
- Consideration of pharmacologic agents for chronic administration.
Main Results:
- Therapies reducing cell death during ischemia show promise for limiting infarct size.
- Regenerative approaches, including extracellular matrix, may aid in reducing left ventricular remodeling.
- A dual therapeutic approach targeting both acute infarct size reduction and chronic remodeling is proposed.
Conclusions:
- Reducing myocardial cell death during ischemia is a key strategy to limit infarct size.
- Therapies promoting favorable left ventricular remodeling are essential for long-term cardiac function.
- A combined approach, addressing both acute injury and chronic healing, offers the most effective means to preserve cardiac structure and function after myocardial infarction.
Abstract:
While progress has been made in improving survival following myocardial infarction, this injury remains a major source of mortality and morbidity despite modern reperfusion therapy. While one approach has been to develop therapies to reduce lethal myocardial cell reperfusion injury, this concept has not translated to the clinics, and several recent negative clinical trials raise the question of whether reperfusion injury is important in humans undergoing reperfusion for acute ST segment elevation myocardial infarction. Therapy aimed at reducing myocardial cell death while the myocytes are still ischemic is more likely to further reduce myocardial infarct size. Developing new therapies to further reduce left ventricular remodeling after the acute event is another approach to preserving structure and function of the heart after infarction. Such therapy may include chronic administration of pharmacologic agents and/or therapies developed from the field of regenerative cardiology, including cellular or non-cellular materials such as extracellular matrix. The optimal therapy will be to administer agents that both reduce myocardial infarct size in the acute phase of infarction as well as reduce adverse left ventricular remodeling during the chronic or healing phase of myocardial infarction. Such a dual approach will help optimize the preservation of both cardiac structure and function.
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